Report on Health Consequences of Wood Smoke

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Executive Summary

Recent studies on the emissions of wood burning reveal that in most

northern U.S. cities, wood smoke is a significant contributor to overall

community air pollution. The same is true in the urban areas of the

Wasatch Front. If wood smoke were evenly distributed throughout the

airshed, it would be roughly quantitatively equivalent to all vehicle

emissions in the same region. But wood smoke is not evenly distributed. It

concentrates heavily near its sources, subjecting neighbors to

extraordinarily high levels of a wide range of toxic pollution components,

and it has an extremely high “intake fraction,” meaning human exposure is

disproportionately greater than average atmospheric concentrations.

Moreover, wood smoke itself is uniquely toxic, probably more so than any

other common type of urban pollution. As a result, it deserves special

attention from lawmakers and regulators beyond what would be warranted

within the context of a PM2.5 State Implementation Plan (SIP) control

strategy or its contributions to the exceedance of National Ambient Air

Quality Standards (NAAQS). Any public policy incentivizing the trading in of

old wood stoves for newer “EPA-certified” stoves as a substitute for burning

bans is misguided and inadequate, because homeowners will still be left

with heating devices that are far more polluting than other alternatives.


Utah Physicians for a Healthy Environment (UPHE) is the largest civic

organization of health care professionals in Utah, with about 340 members

whose areas of expertise include virtually every medical specialty and

related disciplines such as biology, genetics, chemistry, toxicology,

ecology, atmospheric modeling, and engineering. The health effects of air

pollution represent the core of our expertise and therefore our engagement

in public policy. UPHE has made note of the withdrawal of the woodburning

ban proposal by Governor Gary Herbert and the Utah Division of

Air Quality. Nonetheless, UPHE wishes to register this report with the Utah

Air Quality Board (AQB) in support of the proposal, and in fact raise issues

associated with the burning of solid fuel that were not addressed by the


A strong case can be made that air pollution is the largest public health

threat in most urban areas and with more consequence than smoking.

Every breath that every person takes—including pregnant women, infants,

and children—is contaminated by air pollution to some degree. In contrast,

smoking is limited to a fraction of the population, and even smokers only

inhale cigarette smoke during a small percentage of their total daily

respirations. Worldwide deaths due to cigarette smoking are estimated at 5

million per year,85 and the World Health Organization (WHO) estimates air

pollution kills 8 million people per year.86 Furthermore, smoking is

“voluntary” air pollution exposure, while community air pollution is primarily

involuntary; this is particularly true in the case of wood smoke.

Air pollution in general is increasingly recognized as a systemic health

threat, impairing the functioning of virtually every organ system, and related

to the same broad spectrum of disease outcomes as cigarette smoke.

Because of this, UPHE proposes for consideration by the AQB a rule that

would address wood burning by residents, restaurants, unregulated

incinerators used by small businesses, and the growing popularity of

essentially unregulated household incinerators, only under a new name

that suggests a desirable property amenity—“backyard fire pits.”

Burning trash in backyard incinerators has long been prohibited in most

urban areas, and the justification is obvious. Operating a vehicle with

excessive emissions has long been prohibited through emissions

inspections. The rationale has been accepted that even though it may be

cheaper for the owner of an older, more polluting vehicle to continue to

operate that vehicle, for the public good those vehicles must be cleaned up

or retired. Why should home heating devices be any different?

Furthermore, comparing wood-burning devices used during the winter

season to auto emissions, by various metrics it is a fair approximation that

one household burning wood all winter produces as much pollution as

between 90 to 400 automobiles driven all winter.1 So while we have long

had in place a regulatory mechanism to limit how much pollution one

vehicle may emit, we have had no mechanism to limit how much pollution

one home may emit, despite the potential for it being a much larger source

of pollution.

Many years ago our society adopted a the norm that no one should be

involuntarily subjected to secondhand cigarette smoke because of the

inherent public health consequences and the infringement on the rights of

nonsmokers to avoid exposure. Routine wood-burning in an urban setting

should not be allowed for exactly the same philosophical, aesthetic and

public health reasons as prohibition of cigarette smoking in public venues,

backyard trash incineration, and excessive vehicle emissions. The smoke

from wood stoves, fire pits, boilers and fireplaces creeps onto adjacent

property and into nearby homes, affecting the quality of life and health of

neighbors. Cheap heat or pleasant ambiance for a resident burning wood is

engaged in at the expense of nearby neighbors and the community at

large, just like secondhand cigarette smoke.

1. Wood smoke is a surprisingly large contributor to

overall community pollution levels.

Wood burning has an enormous impact on community-wide pollution

levels. Source apportionment studies have estimated that wood/biomass

combustion contributes 10 percent to 60 percent of the fine-particle

concentrations (PM2.5) in large cities, such as Seattle, Phoenix, Beijing,

Prague and Helsinki.2,3,4,5 In Pierce County, Washington, 53 percent of

PM2.5 emissions comes from wood. A study in Los Angeles showed that in

the winter, residential wood combustion there contributed 30 percent of

primary organic aerosols (probably the most important mass component of

particulate pollution), more than motor vehicle exhaust, which contributed

21 percent.6,7 In Fresno, California, wood smoke contributed on average 41

percent of organic carbon and approximately 18 percent of total PM2.5

mass.8 A study in two San Jose, California, locations showed that wood

smoke pollution was 4.4 times that of gasoline- or diesel-fueled vehicles.104

There is no reason to think that Utah’s largest cities would be much

different. In fact, the common figure recited by the media, and even the

governor—that wood smoke is “5 percent” of the problem—is a complete

misunderstanding and/or mischaracterization of the “the problem.” The

source of the “5 percent” number is a study published by AQB member

Kerry Kelly.9 About one-third of the total PM2.5 emissions is “primary;” the

rest is “secondary” (formed in the atmosphere from precursor gases).

About one-third of the primary PM2.5 emissions was from wood burning

and cooking combined—specifically, 38 percent, compared to 35 percent

for all cars and trucks when the PM2.5 emissions was above 20 μg/m3. If

residential wood burning is half of the wood/cooking inventory, 5 percent is

the result of 1/3 x 1/3 x 1/2. So while 5 percent seems like a small number,

the study shows residential wood burning and grilling are as much of the

“problem” as all of our vehicles. But the bulk of medical research indicates

that “primary” PM2.5 emissions are much more toxic than “secondary”

PM2.5 emissions, making the real threat much greater than “5 percent”

suggests. This study further speaks to the inadequacy of the current woodburn curtailment program in controlling the problem.

A recent program initiated in the San Joaquin Valley Air Basin (SJVAB) to

reduce wood smoke demonstrated an improvement in air quality related to

even a modest program to reduce wood burning. Within three years, a

reduction of 15 percent in PM2.5 levels and 13 percent in hospitalizations

for ischemic heart disease was achieved in their urban areas.97 Bear in

mind, this program did not incorporate a season-long ban, and the average

wintertime temperatures in the SJVAB are ten degrees warmer than in Salt

Lake City. Therefore, any program to reduce or ban wood smoke in Utah’s

urban areas would undoubtedly achieve even greater reductions.

According to the California Environmental Protection Agency Air Resources

Board, the inhalable particle pollution from one wood stove is equivalent to

the amount emitted from 3,000 gas furnaces producing the same amount of

heat per unit. While so-called EPA-certified wood stoves might burn

cleaner, they cannot begin to approach the much lower emissions levels of

natural gas furnaces.

2. Wood smoke is not evenly distributed throughout the airshed.

Severe hot spots of pollution and “local victims” are created.

A study in Seattle during winter months showed much higher increases in

particulate pollution in residential areas where wood burning occurred,

compared to the business district—67 percent compared to 9 percent.10

Another study revealed that about 90 percent of fine particulate pollution in

a Tacoma neighborhood came from wood burning.11, An EPA study states

that “In some neighborhoods, on some days, 90% of the particle pollution is

from residential wood burning.” 103

Unlike most other sources of pollution, wood-burning emissions in a home

are released directly into the area where people spend most of their time,

at an elevation that does not promote dispersion. A recent study in Finland

confirmed both the greater impact of wood burning compared to vehicle

emissions and the concentration effect near its sources.108 Studies from

California show that within a single square kilometer of a residential area,

concentrations of wood smoke can vary as much as 2,500 times.12 The

highest measured concentrations were up to 100 times higher than the

community average. A single wood-burning household can envelope

adjacent and downwind homes with a primary PM0.1 (the most dangerous

subset of PM2.5) plume. This demonstrates how significant the creation of

“local victims” is in assessing the true extent of the health impacts of wood

burning. Smoking on airplanes or in public buildings is not prohibited

because of what that does to community PM2.5 levels. It is prohibited

because of the direct public health consequences to those in the immediate

area. The same consideration and protection should apply for neighbors in

the issue of wood burning to prevent “local victims.”

“The largest single source of outdoor fine particles (PM2.5) entering into

our homes in many American cities is our neighbor’s fireplace or wood

stove. … Only a few hours of wood burning in a single home at night can

raise fine-particle concentrations in dozens of surrounding homes

throughout the neighborhood and cause concentrations of PAHs (polycyclic

aromatic hydrocarbons)—one of the most toxic compounds of air pollution

—higher than 2,000 ng/m3.” (Dr. Wayne Ott, Stanford University, Feb. 1,

1998). Background concentrations of PAHs should be close to zero.

Wood smoke is not just an outdoor problem. In houses without current

wood burning, fine-particle levels are usually lower than outdoor levels. But

in areas with high levels of wood smoke, even houses not using wood

stoves or fireplaces have higher indoor wood smoke levels. Wood smoke

particles are very small (ultrafine), ranging from 0.2 microns at the start of

the burn period to .05 microns as the burn cycle progresses. Particles of

this size behave like gases. There is no practical way to prevent wood

smoke pollution from seeping into nearby homes. The extremely small size

of the particles results in the particles remaining suspended in the

atmosphere for long periods of time, making a disproportionate contribution

to airshed pollution. Stagnant conditions and winter temperature inversions

result in wood smoke hanging close to the ground, easily penetrating

homes and buildings.

A study by the University of Washington showed that 50 percent to 70

percent of the outdoor levels of wood smoke were found in nearby homes

that were not burning wood. The EPA did a similar study in Boise, Idaho,

with similar results.13 A study in California showed an even higher result:

Indoor wood smoke was found to average 88 percent, as high as outdoors.

1 If a homeowner follows current Salt Lake County rules recently

established by the Salt Lake County Board of Health, and doesn’t burn

during “yellow” or “red” alerts days, but does burn during all “green” days,

his/her neighbors can go an entire winter without having even one day of

clean air.

An important concept in pollution and public health is that of population

“intake fraction.” Intact fraction is the mass of pollutant inhaled divided by

the mass emitted. Obviously, regarding health consequences, what is

inhaled is what matters, much more so than what is emitted. Two different

pollution sources with comparable emission rates of the same pollutant can

have significantly different intake fractions, depending on the surrounding

population density and the juxtaposition of the point of release. Wood

smoke has a uniquely high intake fraction. During the winter, people spend

about 90 percent of their time indoors, and most of that time is spent in

their own homes. Residential wood smoke is the only major pollution

source that is released exactly in the area where people spend most of

their time, at a height where dispersion is minimal. Some pregnant women

and some children spend even more of their time at home. For many

physiologic, metabolic and developmental reasons, children and fetuses

are well known to be much more sensitive to pollution’s health impacts,

with the potential for long-term health impacts. The public health

consequences of in-home and neighborhood wood smoke are magnified

further because many members of the most vulnerable subset of the

population are the most exposed.

The concept of “intake fraction” raises a troubling irony—people who burn

wood are their own worst victims, subjecting themselves and especially

their children (more than anyone else) to increased pollution levels.

Particulate levels were found to be from 26 percent14 to as much as 500

percent higher in the indoor air of wood-burning homes compared to non–

wood-burning homes,15 and levels far beyond “red alert” conditions.

Benzene levels were 29 percent higher.16 Average levels of the highly toxic

PAHs were 300 percent to 500 percent higher.17

Children living in homes where wood is regularly burned were much more

likely to have severe respiratory symptoms compared to non–wood-burning

controls.18 Children in Klamath Falls, Oregon, showed decreases in lung

function during the wood-burning season in those parts of the city with the

highest amount of wood-burning.19 Numerous studies of adults show the

same general trend of increased symptoms of respiratory disease among

those living in residences with fireplaces or wood stoves in use.

Wood boilers deserve special mention and condemnation as severe health

hazards because of their shockingly high pollution results. In a 2006 report

from Northeastern States for Coordinated Air Use Management

(NESCAUM), wood boilers were found to produce PM2.5 levels over 1,000

μg/m3 periodically, with frequent values over 400 μg/m3 during routine

operation of the boiler, with levels measured up to 150 feet away. Peak

levels measured at 50, 100, and 150 feet from the stack often reached over

4,000 μg/m3, including an astounding 8,800 μg/m3 peak measurement at

50 feet away.

3. Wood smoke is even more toxic than other particulate pollution.

The Canadian government’s official website, Healthy Canadians, states

boldly and unequivocally, “Avoid Wood Smoke.”96 Wood smoke is an

extreme public health hazard, containing over 200 toxic chemicals and

compound groups. The emissions from wood smoke are almost entirely in

the inhalable size range.20 A study in Vancouver reported that wood smoke

particles are seven times more likely to be breathed into our lungs than the

average PM2.5 particle in Vancouver’s air.21,22 Once inhaled, the small

particles that are characteristic of wood smoke also more easily penetrate

cell walls and even subcellular structures, such as mitochondria and the

cell nucleus.87 It is at this microscopic, cellular level that particulate matter

triggers its broad array of health consequences.

Components of wood smoke are similar to those of cigarette smoke. Both

types of smoke include particulate matter, carbon monoxide, formaldehyde,

sulfur dioxide, nitrogen oxides, dioxins, and polycyclic aromatic

hydrocarbons (PAHs).23 Furthermore, as with cigarettes, those who are

doing the wood burning are the most victimized by the pollution generated.

A report by Environment & Human Health, Inc., “The Health Effects of

Wood Smoke,” cites medical research indicating that wood smoke

interferes with lung development in children and increases a child’s risk for

serious lower respiratory infections, such as bronchitis and pneumonia.24

Wood smoke exposure can depress the immune system, damage the

pulmonary epithelium25 and increase arterial stiffness.26

The very small size of the particulate emissions and high levels of PAHs

from wood smoke may account for its excessive toxicity compared to fossil

fuel-generated particulate matter. Ultrafine particles are more potent in

inducing inflammatory responses in the human body than fine particles.

27,28,29,30,31,32 Wood smoke produces high levels of free radicals, leading to

DNA damage as well as inflammatory and oxidative stress responses in

gene expression in cultured human cells.33,34 Exposure to PAHs has been

associated with mutations in tumor suppressor genes.

The federal Environmental Protection Agency estimates that the lifetime

cancer risk from wood stove smoke is twelve times greater than that from

an equal volume of secondhand tobacco smoke. (The Health Effects of

Wood Smoke, Washington state Department of Ecology). Organic extracts

of ambient particulate matter containing substantial quantities of wood

smoke are 30-fold more potent than extracts of cigarette smoke

condensate in a mouse skin tumor-induction assay that was conducted.35

Wood smoke exposure approximately doubles an individual’s risk of getting

lung cancer92,93 and cancers of the mouth and throat.94 One study showed

a significant increase in childhood brain tumors with prenatal and postnatal

exposure to wood smoke.90 PAH attachment to DNA (DNA adducts) has

been specifically correlated with higher rates of breast cancer.

Studies of cigarette smoke and automobile traffic-generated pollution show

that significant epigenetic changes, e.g., genotoxicity, can occur literally

within minutes or hours after exposure,83,84 so there is every reason to

believe that wood smoke would act just as quickly. Smokers exposed to

wood smoke, either through home heating andcooking or through

neighborhood pollution, are not only at increased risk of chronic obstructive

pulmonary disease (COPD), but they are also more likely to have

epigenetic changes in their DNA that synergistically increases their risk of

COPD and related pulmonary problems, and likely also lung cancer.91

Wood smoke particles have been reported to induce DNA damage in vitro

in human monocytic and epithelial cell lines and in a murine macrophage

cell line. However, particles from poor combustion—e.g., low-temperature

wood boilers and other inefficient wood-burning appliances—seem to have

greater effects on both cytotoxicity and DNA damage than particles from

more complete combustion conditions.88,89


Free radicals produced from wood smoke are chemically active for twenty

minutes. In contrast, tobacco smoke free radicals are chemically active for

thirty seconds. Wood smoke free radicals may attack our body’s cells up to

forty times longer once inhaled.36 Animal toxicology studies show that

wood smoke exposure can disrupt cellular membranes, depress

macrophage activity, destroy ciliated and secretory respiratory epithelial

cells, and cause aberrations in biochemical enzyme levels.37


Undoubtedly, making a major contribution to the toxicity of wood smoke is

the high concentrations of PAHs. The EPA estimates that a single fireplace

operating for one hour, burning ten pounds of wood, will generate more

PAHs than 6,000 packs of cigarettes.38 Other estimates indicate an even

higher rate of PAH release.39,40 Wood burning is the largest source of

PAHs in the urban environment. In urban circumstances where wood

burning is common in the winter, atmospheric PAH concentrations can be

15 times higher during the winter than during the summer.100,101

Furthermore, wood-burning appliances with similar emission profiles for

particulate matter may simultaneously produce dramatically different

amounts of PAHs.41

Adverse health effects far beyond carcinogenicity add to the need for

community control strategies to reduce wood smoke, which should be a top

priority in any overall pollution reduction strategies.

PAHs have been implicated in numerous studies showing adverse

pregnancy outcomes and impaired fetal development, including birth

defects. Prenatal exposure to PAHs has been found to adversely change

placental vascular architecture, trigger pro-carcinogenic epigenetic

changes, and is associated with decreased intelligence, higher rates of

behavioral and attention deficit disorders, and obesity.42,43,44,45,46,47,48,49,50

DNA damage induced by PAH exposure has been demonstrated by

numerous studies. Fetuses are far more susceptible to DNA damage and

pro-carcinogenic epigenetic changes than are adults.95

A remarkable new study showed a direct linear relationship between the

amount of PAH exposure during pregnancy and MRI scans that

documented loss of volume in brain white matter and loss of intelligence

and behavioral disorders in children 110

Furthermore, PAH from wood smoke will land on indoor household and

outdoor surfaces and soils, resulting in second- and third-hand ingestion

and skin absorption. Studies done in soil near oil refineries (whose

emissions are also high in PAHs) have shown concentrations as high as

200,000 μg/kg.51


A complete review of the toxicity of the group of chemically related

compounds called dioxins is beyond the scope of this review. Nonetheless,

dioxins deserve special mention. Wood smoke is the third largest source of

dioxin exposure in the United States.52 Dioxin levels are typically measured

in picograms, one trillionth of a gram. Burning just one kilogram of wood

produces as much as 160 micrograms of dioxins.53

An Australian study found that wood heaters were responsible for

increasing background dioxin concentrations by ten times compared to

during the non-heating season.54 The burning of wood pellets and other

forms of treated wood has the potential to release even higher

concentrations of dioxins. Copper, a common biocide element that is

chemically bound to wood, is an important dioxin catalyst. Preservative

metals promote smoldering of wood char following the cessation of flaming,

providing the required temperature environment for dioxin formation, and

chlorinated organics added as secondary preservative components yield

dioxin precursors upon thermal decomposition.55

Dioxins are among the most toxic compounds to which humans can be

exposed. Dioxins, and many of the other chemicals in wood smoke, are

exactly the type of chemicals that the American College of Obstetricians

and Gynecologists and the American Society for Reproductive Medicine

addressed in a prepared statement in autumn 2014.

“Reducing exposure to toxic environmental agents is a critical area of

intervention for obstetricians, gynecologists, and other reproductive

health care professionals. Patient exposure to toxic environmental

chemicals and other stressors is ubiquitous, and preconception and

prenatal exposure to toxic environmental agents can have a profound

and lasting effect on reproductive health across the life course.

Prenatal exposure to certain chemicals has been documented to

increase the risk of cancer in childhood…[we] join leading scientists

and other clinical practitioners in calling for timely action to identify and

reduce exposure to toxic environmental agents while addressing the

consequences of such exposure.”56

Dioxins fall into the broad category of endocrine disruptor chemicals. The

Endocrine Society, internal medicine specialists in diseases of the

pancreas, thyroid, adrenal and pituitary glands, and hormone dysfunction,

issued this statement about dioxins in 2010:

“Even infinitesimally low levels of exposure indeed, any level of

exposure at all, may cause endocrine or reproductive abnormalities,

particularly if exposure occurs during a critical developmental window.

Surprisingly, low doses may even exert more potent effects than higher


Dioxins, like PAHs, are a particularly significant threat to fetuses and

infants. Greater levels of dioxin exposure are associated with pregnancy

loss and pre-term delivery,58 impaired fetal growth and smaller birth size,

including smaller head size.59 Dioxins also cause immunosuppression.

Prenatal exposure is associated with a 250 percent to 500 percent increase

in episodes of otitis media in 18-month-olds.60 Many chemicals, such as

dioxins, have been shown to not only impair the health of those exposed

but through epigenetic changes to also impair the health of subsequent

generations who are not exposed.61


Acrolein is a chemical found in high concentrations in both cigarette and

wood smoke. Acrolein is well known to suppress the immune system62 and

has recently been strongly implicated in demyelinating diseases, such as

multiple sclerosis.63,64 The authors of a recent study stated, “We think that

acrolein is what degrades myelin. … We’ve discovered that acrolein may

play a very important role in free radical injury, particularly in multiple

sclerosis.” One day’s worth of wood burning for an average household

produces as much acrolein as 26,000 cigarettes.

Several studies suggest that particulate pollution in wood smoke from

wildfires is much more toxic to lung macrophages than an equivalent

concentration of similarly sized particulate pollution found in typical urban

smog.65,66,67,68 A recent study demonstrated lower birth weights among

babies born to mothers who were pregnant during a two-week stretch of

severe wildfires in Southern California.69

A study of a population in Peru demonstrated significantly higher blood

pressures among those living in homes that burned wood, compared to

those that didn’t. Wood and other biomass fuel users had systolic blood

pressures that averaged seven mmHg higher, and diastolic blood

pressures that averaged almost six mmHg higher compared to nonburners.

That is a remarkable difference, and, considering all the

consequences of a higher blood pressure, one to have serious

consequences for all cardiovascular related health complications.109

Another recent study compared daily hospital admissions and death rates

related to cardiovascular and pulmonary diseases in two cities in South

America where one city’s pollution was predominantly from wood smoke

and pollution in the other was from mobile and typical point sources.

Compared to the non–wood-burning city, the city with primarily wood

smoke experienced an increase of 47 percent for cardiorespiratory deaths

and an increase of 104 percent for respiratory hospital admissions for every

10 μg/m3 increase in PM10.70

4. “EPA-certified stoves” are not the solution.

“No natural gas service” is no longer an excuse.

Not surprisingly, the Hearth, Patio and Barbecue Association (HPBA) has

been mounting a campaign to not only fight any banning of wood burning

but also to convince policy makers that the answer to wood smoke is to sell

more of their product, not less. Below are eight reasons that policy makers

should not accept this rationale.

1. EPA stove performance in the real world does not match their

performance as tested in the lab, something that the manufactures and

the EPA acknowledge.71,72 For example, current testing standards

specify the use of kiln dried lumber precisely arranged in a crib formation

—hardly representative of the way most stoves are actually operated.

Emission rates reported in the certification process do not represent

emission levels of stoves in homes after extended use.

The wood-burning-device industry (HPBA) and the EPA claim that wood

stoves emit 70 percent less particulate matter, and therefore the answer

to community problems with wood burning is to sell more of these

products, not ban them. However, the EPA’s program in Libby, Montana,

is proof in the real world that those claims are exaggerated. The woodburning

industry, the EPA and the state paid to change out every wood

stove in the Libby area to an EPA-certified stove. They also invested in

education programs and proper installation. Yet using industry’s own

numbers from an industry-funded study, particulate matter (PM) was

reduced by only 28 percent. If EPA stoves performed as claimed, PM

reduction should have been 56 percent. Before the change-out, 83

percent of Libby’s winter PM came from residential wood burning. If the

subsidies had gone to change to propane or electric heat, PM levels

would have dropped almost 80 percent, while also reducing toxics and


Another change-out study in Idaho found that almost 33 percent of the

homes where EPA-certified stoves replaced older models showed

increases in indoor particulate matter.73 A study prepared for the EPA

showed that after extended use, actual emissions were over three times

greater than the certified values.74

The consistency and reproducibility of wood-heater emissions testing is

very poor. Many relatively small, uncontrollable variables that are

inherent in the wood combustion process, such as type of wood,

substrate configuration and moisture content, can combine to

significantly affect the outcome of any given test.75 The emissions from

modern combustion appliances for wood logs may increase 10-fold if

they are not operated appropriately.76

2. Wood stoves generate a large amount of emissions when they are

started up, but these emissions are not “counted” in the EPA testing

procedure. Testing does not begin until the stove has begun to burn


3. EPA wood stoves have never been shown to reduce the amount of the

most deadly components of wood smoke, including dioxins, furans, and

PAHs. Some studies have shown that EPA stoves emit even more of

these highly toxic compounds.77,78,79

4. In-home performance is too dependent on the operator—airflow and fuel

choice radically affect the actual emissions. A stove poorly operated or

maintained can emit ten times more pollution than lab testing indicates.

John Gulland, manager of the “pro-wood” Wood Heat Organization, puts

it this way: “People who don’t care about the impacts of their actions on

neighbors and are content to remain ignorant of good wood-burning

practice will make a lot of smoke, regardless of the emissions rating of

the appliance they choose.”80

5. Typical wood-stove operation employs “dampering down” at bedtime or

during temperate weather. Since oxygen is a necessary component of

combustion, this can create much higher levels of pollutants.

6. The performance of wood-heating devices equipped with catalytic

components degrades over time—if poorly maintained, in as little as two

years.98 Structurally, wood heaters also degrade with use, and emission

factors increase. The negative consequences of degraded catalytic

components, which can include dramatically increased emissions, occur

outside the end-user’s home. Thus, there is no reason to think that

owners will replace the degraded catalytic components or expend the

effort and money to maintain them properly.81

7. Even if wood stoves and their pollution control devices did not degrade

over time and if they were all operated the way they are tested in the lab,

they are still hundreds of times dirtier than a natural gas furnace in

emitting particulate pollution and even more so in emitting hazardous air

pollutants (dioxins, furans, PAHs and heavy metals).

8. Exempting supposedly “cleaner” stoves from any wood-burning ban

would only make sense if combined with emissions verification by actual

testing in the field on a regular basis, just like how cars are tested. That

would be difficult, impractical and costly but is likely to produce greater

pollution reductions than the current vehicle emissions program.

Emissions checks could be paid for by a licensing fee like the one

required for automobiles.

Lack of natural gas service is no longer an excuse to have to burn wood.

From a report from Families for Clean Air99:

“The reliance on wood burning for home heating in these areas is

rationalized on the basis that the cost of electric heat or propane is

too expensive. This rationale has even held sway with air quality

regulators, who have exempted areas not serviced with natural gas

from wood burning restrictions on days when the air quality is poor or

predicted to be poor.

“But now, thanks to advances in technology, heating a home with an

electric split ductless heat pump is cheaper than heating with natural

gas. Split ductless heat pumps are extremely efficient because they

move heat from one place to another rather than generating heat

from energy. Installation does not require ductwork, which can be

expensive and difficult to put in. In fact, the cost to purchase and

install a split ductless unit is comparable to the purchase and

installation of a wood stove. Note that these split ductless heat pump

units can cool as well as heat.

5. Inversion season is not the only time we are at

risk from wood smoke.

There is no safe level of air pollution. Medical research has well established

that one unit of air pollution emitted into the community airshed when levels

are relatively low has as much, or even greater, health impact as when PM

or ozone concentrations are higher. In fact, plotting a curve correlating

sudden cardiac death (the signature outcome of PM exposure) vs.

concentration of PM yields a curve whose steepest part is at the lowest

doses.82 In other words, eliminating wood burning in circumstances that

already meet the NAAQS may be even more important in protecting public

health. This is not factored into NAAQS, but it is nonetheless an important

consideration in regulating the creation of wood smoke.

The Bay Area Air Quality Management District estimates that more than $1

billion worth of medical expenses are caused by burning wood smoke in

the Bay Area, including the calculation that one wood fire can cost your

next-door neighbor an average of $40 in medical expenses.

6. Wood smoke is a large community economic liability,

and it contributes significantly to global warming.

The Bay Area Air Quality Management District estimates that more than $1

billion worth of medical expenses are caused by burning wood smoke in

the Bay Area, including the calculation that a single wood fire can cost your

next-door neighbor an average of $40 in medical expenses.

Given the overwhelming scientific consensus regarding a growing, primarily

human-caused climate crisis, it is also important to consider the carbon

footprint of wood burning. The 2007 Nobel Prize-winning Intergovernmental

Panel on Climate Change (IPCC), consisting of approximately 2,000

scientists, concluded that black carbon soot, which is a major component of

wood combustion, is a significant “forcer” of global warming. However, a

2013, 232-page report from 31 international scientists using data collection

over four years105 concluded that the real global-warming impact of black

carbon soot was double that of previous estimates. In fact, black carbon

particulates may have a warming effect two-thirds as great as CO2.

Black carbon exerts multiple effects, depending on complex altitude and

atmospheric conditions. Black soot particles on snowpack decrease the

reflection of sunlight and cause atmospheric warming and accelerated melt

of snowpack, which is essentially a loss of available water. Dust from the

Southwest has already been shown to hasten the melting of snow in the

Rocky Mountains, reducing the amount of runoff into the upper Colorado

River by 5 percent, ultimately causing a loss of 250 billion gallons of water

a year.106,107 All particulate matter emitted along the Wasatch Front,

including that from wood burning, will have the same type of effect on

Wasatch Front snowpack, aggravating our water supply woes.

Black carbon particles heat up the layer of the atmosphere where clouds

are forming, promoting cloud evaporation, no longer allowing sunlight to be

reflected back into space. Black carbon also has cooling effects, but

considering both the warming and cooling effects, the amount of extra

energy stored in the atmosphere due to black carbon is 1.1 watts per

square meter of the earth’s surface.105 The same calculation for CO2 is

1.56—particulate pollution has two-thirds the impact of CO2.

A 2010 study concluded that the amount of carbon released per unit of

energy produced is actually greater for wood than it is for fossil fuels. It is a

common misconception that burning wood is carbon neutral. Considering

the entire carbon life cycle of wood, burning releases carbon now when we

can least afford to do so—carbon that would otherwise have been stored

for decades or perhaps centuries. While sustainable forestry practices can

help repay that “carbon debt,” those benefits do not accrue until the distant

future, too late to be of much help. As a result of this study, the state of

Massachusetts changed its renewable portfolio standard to exclude

biomass projects with long carbon payback periods.

The UN Environment Program and the World Meteorological Organization

recommended phasing out log-burn ing stoves in developed countries to

reduce global warming as well as dangerous air pollution. 111 Even if the

wood is from a sustainable source, methane and black carbon emissions

from log-burning stoves cause more global warming than a gas heater or

electric heat pump. 112


We believe that government agencies have the authority—indeed the

obligation—to make rules regarding wood-burning devices stricter than

current rules. The fact that these wood-burning devices already exist, that

companies make a profit manufacturing them, and that many people

choose to use them for reasons such as cost, convenience, or ambiance, is

no excuse for government agencies not to fulfill their obligation to protect

public health. Frankly, federal, state and local governments cannot protect

wood-burning manufacturers and wood burners and simultaneously protect

public health, and it is clearly mandated to do the latter.

It is long overdue for us to consider that subjecting one’s neighbors to the

high pollution consequences of wood-burning devices is as much of an

anachronism as allowing cigarette smoking on airplanes. The medical

science demands that the EPA act aggressively to curtail, as much as is

legally possible, this serious public health menace.


Brian Moench, MD

President, Utah Physicians for a Healthy Environment (UPHE)

Tim Wagner

Executive Director, UPHE

Cris Cowley, MD

Vice President, UPHE

Howie Garber, MD

Board Member, UPHE

Rich Kanner, MD

Board Member, UPHE

Ellie Brownstein, MD

Board Member, UPHE

Todd Seymour, MD

Board Member, UPHE

Michael Woodruff, MD

Board Member, UPHE

Gar Kunkel

Board Member, UPHE


1. Todd JJ. Review of literature on residential firewood use, wood-smoke

and air toxics. Australia. Environment Australia.

2. Wu CF, Larson TV, Wu SY, Williamson J, Westberg HH, Liu LJ: Source

apportionment of PM(2.5) and selected hazardous air pollutants in Seattle.

Sci Total Environ 2007, 386:42-52.

3. Song Y, Tang X, Xie S, Zhang Y, Wei Y, Zhang M, Zeng L, Lu S: Source

apportionment of PM2.5 in Beijing in 2004. J Hazard Mat 2007, 146:124-130.

4. Lewis CW, Norris GA, Conner TL, Henry RC: Source apportionment of

Phoenix PM2.5 aerosol with the Unmix receptor model. J Air Waste Manag

Assoc 2003, 53:325-338.

5. Saarikoski SK, Sillanpää M, Saarnio KM, Hillamo RE, Pennanen AS, Salonen

RO: Impact of biomass combustion on urban fine particulate matter in central and

northern Europe. Water Air Soil Pollut 2008, 191:265-277.

6. Rogge, W. F., L. M. Hildemann, M. A. Mazurek, G. R. Cass, and B. R. T.

Simoneit. (1991) Sources of fine organic aerosol, 1, Charbroilers and meat

cooking operations, Environ. Sci. Technol., 25, 1112–1125.

7. Rogge, W. F., L. M. Hildemann, M. A. Mazurek, G. R. Cass,and B. R. T.

Simoneit. (1998) Sources of fine organic aerosol, 9, Pine, oak and synthetic log

combustion in residential fireplaces, Environ. Sci. Technol., 32, 13–22.

8. Gorin, C, J. Collett, and P. Herckes. (2006) Wood Smoke Contribution to

Winter Aerosol in Fresno, CA. Journal of the Air and Waste Management

Association 56: 1584-1590 (quote on p. 1584).

9. K.E. Kelly, R. Kotchenruther, R. Kuprov, G.D. Silcox, Receptor model source

attributions for Utah’s Salt Lake City airshed and the impacts of wintertime

secondary ammonium nitrate and ammonium chloride aerosol. Journal of the Air

& Waste Management Association, 63:5, 575-590.

10. Hopke PK, Hwang I, Kim E, Lee JH. Analyses of PM-Related Measurements

for the Impacts of Ships. Final Report to the California Air Resources Board,

Contract No. 04-326. September, 2006. 210 p.

11. Ogulei D. Sources of Fine Particles in the Wapato Hills-Puyallup River Valley

Nonattainment Area: Draft Report. Washington State Department of Ecology, Air

Quality Program. Olympia, WA. January, 2010.

12. Thatcher, T. & Kirchstetter, T. (2011). Assessing Near-Field Exposures from

Distributed Residential Wood Smoke Combustion Sources. Report prepared for

the California Air Resources Board.

13. New Hampshire Department of Environmental Services – Air Resources

14. Molnár P, Gustafson P, Johannesson S, Boman J, Barregard L, Sällsten G.

2005. Domestic wood burning and PM2.5 trace elements: Personal exposures,

indoor and outdoor levels. Atmospheric Environment 39(14): 2643-2653

15. Robin, L. F., Less, P. S., Winget, M., Steinhoff, M., Moulton, L. H.,

Santosham, M., and Correa, A. 1996. Wood-burning stoves and lower respiratory

illnesses in Navajo children. Pediatr. Infect. Dis. J. 15(10):859–865.

16. Gustafson P, Barregard L, Strandberg B, Sällsten G. 2007. The impact of

domestic wood burn- ing on personal, indoor and outdoor levels of 1,3-butadiene,

benzene, formaldehyde and acetaldehyde. J Environ Monit. 9(1):23-32

17. Gustafson P, Ostman C, Sällsten G. 2008. Environ Sci Technol. 42(14):

5074-80. Indoor levels of polycyclic aromatic hydrocarbons in homes with or

without wood burning for heating

18. Honicky, R. E., Osborne, J. S., 3rd, and Akpom, C. A. 1985. Symptoms of

respiratory illness in young children and the use of wood-burning stoves for

indoor heating. Pediatrics 75(3):587–593.

19. Heumann, M., Foster, L. R., Johnson, L., and Kelly, L. 1991. Wood smoke air

pollution and changes in pulmonary function among elementary school children.

Paper read at 84th Annual Meeting of the Air and Waste Managment

Association, June 16–21, at Vancouver, BC.

20. Environmental Impact of Residential Wood Combustion Emissions and Its

Implications, John A. Cooper, APCA Journal, Vol.30 No.8, August 1980

21. Ries et al.. Intake Fraction of Urban Wood Smoke, Envir Sci Tech, 2009

22. Wood Smoke Brochure. Vol. 113, No. 4, April 2005 http://

23. Minnesota Pollution Control Agency


24. Washington State Department of Ecology; Air Quality Program. Smoke



25. Unosson J, Blomberg A, Sandström T, Muala A, Boman C, Nyström R,

Westerholm R, Mills NL, Newby DE, Langrish JP, Bosson JA. Exposure to wood

smoke increases arterial stiffness and decreases heart rate variability in humans.

Part Fibre Toxicol. 2013 Jun 6;10(1):20. [Epub ahead of print]

26. American Lung Association – Air Quality

27. Unosson J, Blomberg A, Sandström T, Muala A, Boman C, Nyström R,

Westerholm R, Mills NL, Newby DE, Langrish JP, Bosson JA. Exposure to wood

smoke increases arterial stiffness and decreases heart rate variability in humans.

Part Fibre Toxicol. 2013 Jun 6;10(1):20. [Epub ahead of print]

28. American Lung Association – Air Quality

29. Brown DM, Stone V, Findlay P, MacNee W, Donaldson K: Increased

inflammation and intracellular calcium caused by ultrafine carbon black is

independent of transition metals or other soluble components. Occup Environ

Med 2000, 57:685-691.

30. Murphy SAM, Berube KA, Richards RJ: Bioreactivity of carbon black and

diesel exhaust particles to primary Clara and type II epithelial cell cultures. Occup

Environ Med 1999, 56:813-819.

31. Höhr D, Steinfartz Y, Schins RPF, Knaapen AM, Martra G, Fubini B, Borm

PJA: The surface area rather than the surface coating determines the acute

inflammatory response after instillation of fine and ultrafine TiO2 in the rat. Int J

Hyg Environ Health 2002, 205:239-244.

32. Monteiller C, Tran L, MacNee W, Faux S, Jones A, Miller B, Donaldson K:

The pro-inflammatory effects of low-toxicity low-solubility particles, nanoparticles

and fine particles, on epithelial cells in vitro: the role of surface area. Occup

Environ Med 2007, 64:609-615.

33. Danielsen PH, Møller P, Jensen KA, Sharma AK, Wallin H, Bossi R, Autrup

H, Mølhave L, Ravanat JL, Briedé JJ, de Kok TM, Loft S. Oxidative stress, DNA

damage, and inflammation induced by ambient air and wood smoke particulate

matter in human A549 and THP-1 cell lines. Chem Res Toxicol. 2011 Feb

18;24(2):168-84. Epub 2011 Jan 14.

34. Karlsson HL, Ljungman AG, Lindbom J, Möller L: Comparison of genotoxic

and inflammatory effects of particles generated by wood combustion, a road

simulator and collected from street and subway. Toxicol Lett 2006, 165:203-211.

35. Cupitt, L. T., Glen, W. G., and Lewtas, J. 1994. Exposure and risk from

ambient particle-bound pollution in an airshed dominated by residential wood

combustion and mobile sources. Environ. Health Perspect. 102(S4):75–84.

36. Lachocki, Pryor, et al, Persistent Free Radicals in Wood smoke, Louisiana

State University, Free Radical Biology & Medicine Vol.12, 1992)

37. Timothy V. Larson and Jane Q. Koenig. A Summary Of Emissions

Characterization And Noncancer Respiratory Effects Of Wood Smoke,

U.S.EPA-453/R-93-036, Dec. 1993

38. 11. Sacramento Metropolitan Air Quality Management District – Agenda,

page 5. MarParticulateMatterSB656Briefing.pdf

39. Ding YS, Trommel JS, Yan XJ, Ashley D, Watson CH. Determination of 14

polycyclic aromatic hydrocarbons in mainstream smoke from domestic cigarettes.

Environ Sci Technol. 2005 Jan 15;39(2):471-8.

40. Naeher L, et al. Woodsmoke Health Effects: A Review. Inhalation Toxicology,

19:67–106, 2007 ISSN: 0895-8378 print / 1091-7691 online DOI:


41. Lamberg H, et al. Physicochemical characterization of fine particles from

small-scale wood combustion. Atmospheric Environment. Volume 45, Issue 40,

December 2011, Pages 7635–7643

42. Rennie MY, Detmar J, Whiteley KJ, Yang J, Jurisicova A, Adamson SL, Sled

JG. Vessel tortuousity and reduced vascularization in the fetoplacental arterial

tree after maternal exposure to polycyclic aromatic hydrocarbons. Am J Physiol

Heart Circ Physiol 300: H675–H684 (2011)

43. Rennie M, et al. Vessel tortuousity and reduced vascularization in the

fetoplacental arterial tree after maternal exposure to polycyclic aromatic

hydrocarbons. Am J Physiol Heart Circ Physiol 300: H675–H684, 2011. First

published December 10, 2010; doi:10.1152/ajpheart.00510.2010.

44. Frederica P. Perera, Deliang Tang, Shuang Wang, Julia Vishnevetsky,

Bingzhi Zhang, Diurka Diaz, David Camann, Virginia Rauh. Prenatal Polycyclic

Aromatic Hydrocarbon (PAH) Exposure and Child Behavior at age 6-7.

Environmental Health Perspectives, 2012; DOI: 10.1289/ehp.1104315

45. Edwards SC, Jedrychowski W, Butscher M, Camann D, Kieltyka A, Mroz E,

et al. 2010. Prenatal Exposure to Airborne Polycyclic Aromatic Hydrocarbons and

Children’s Intelligence at Age 5 in a Prospective Cohort Study in Poland. Environ

Health Perspect :-. doi:10.1289/ehp.0901070

46. Jedrychowski, et al. J Expo Sci Environ Epidemiol, 2013

47. Bocskay, et al. Cancer Epidemiol Biomarkers Prev, 2005

48. Perera, et al. Cancer Epidemiol Biomarkers Prev, 2005

49. Gladen BC, Zadorozhnaja TD, Chislovska N, Hryhorczuk DO, Ken- nicutt

MC, Little RE. Polycyclic aromatic hydrocarbons in placenta. Hum Exp Toxicol

19: 597–603, 2000.

50. Rundle A, et al. Association of Childhood Obesity With Maternal Exposure to

Ambient Air Polycyclic Aromatic Hydrocarbons During Pregnancy. Am J

Epidemiol. 2012 Jun 1; 175(11): 1163–1172. Published online 2012 Apr 13. doi:



52. EPA 1994, Loretta Ucelli spokeswoman, Washington Post

53. Nestrick, TJ and and Lamparski LL. Science, Vol. 266 Oct. 21, 1994, Anal.

Chem. 54, 2292 (1982).

54. Gras J, et al. Dioxins and woodsmoke in Australian cities. Available at: http://

55. Tame N, et al. Formation of dioxins and furans during combustion of treated

wood. Progress in Energy and Combustion Science. Volume 33, Issue 4, August

2007, Pages 384–408doi:10.1016/j.pecs.2007.01.001





58. Tsukimor K, et al. Long-Term Effects of Polychlorinated Biphenyls and

Dioxins on Pregnancy Outcomes in Women Affected by the Yusho Incident.

Environ Health Perspect. 2008 May; 116(5): 626–630. Published online 2008

Feb 6. doi: 10.1289/ehp.10686

59. Tawara K, et al. Effects of maternal dioxin exposure on newborn size at birth

among Japanese mother–infant pairs. Environ Health Prev Med. 2009 Mar;

14(2): 88–95. Published online 2008 Nov 8. doi: 10.1007/s12199-008-0061-x

60. Miyashitaa C, Effects of prenatal exposure to dioxin-like compounds on

allergies and infections during infancy. Environmental Research. Volume 111,

Issue 4, May 2011, Pages 551–558

61. Schmidt C. Uncertain Inheritance: Transgenerational Effects of

Environmental Exposures. Environ Health Perspect; DOI:10.1289/ehp.121-A298

62. Stone R. Environmental toxicants under scrutiny at Baltimore meeting.

(March 1995 Society of Toxicology conference). Science 1995;March 24, v267

n5205 p1770(2).

63. Tully M1, Shi R. New insights in the pathogenesis of multiple sclerosis–role

of acrolein in neuronal and myelin damage. Int J Mol Sci. 2013 Oct 9;14(10):

20037-47. doi: 10.3390/ijms141020037.

64. Leung G, et al. Anti-acrolein treatment improves behavioral outcome and

alleviates myelin damage in EAE mouse. Neuroscience. Jan 26, 2011; 173:


65. Franzi LM, Bratt JM, Williams KM, Last JA. Why is particulate matter

produced by wildfires toxic to lung macrophages? Toxicol Appl Pharmacol. 2011

Sep 16. [Epub ahead of print].

66. Environmental Health Perspectives, California Wildfires of 2008: Coarse and

Fine Particulate Matter Toxicity, 2009, Vol. 117 (6):893-897.

67. Environmental Health Perspectives: Oxidative Punch of Wildfires, 117:A58,

February, 2009.

68. Migliaccio CT, Kobos E, King QO, Porter V, Jessop F, Ward T. Adverse

effects of wood smoke PM(2.5) exposure on macrophage functions. Inhal

Toxicol. 2013 Feb;25(2):67-76. doi: 10.3109/08958378.2012.756086.

69. Kessler, R. et al, “Followup in Southern California: decreased birth weight

following prenatal wildfire smoke exposure.” Environ Health Perspect. 2012 Sept;

120(9): a362

70. Díaz-Robles L, et al. Short Term Health Effects of Particulate Matter: A

Comparison between Wood Smoke and Multi-Source Polluted Urban Areas in

Chile. Aerosol and Air Quality Research, 15: 306–318, doi:10.4209/aaqr.


71. Residential Wood Combustion Technology Review Volume 1. Technical

Report. 1998. Houck and Tiegs (OMNI Environmental Services). Prepared for the


72. EPA Wood Heater Test Method Variability Study: Analysis of Uncertainty,

Repeatability and Reproducibility based on the EPA Accredited Laboratory

Proficiency Test Database. 2010. Curkeet (Intertek Testing Services) and

Ferguson (Ferguson, Andors & Company).

73. Measurable Outcomes of a Woodstove Changeout on the Nez Perce

Reservation [Idaho] Final Report. 2009, By Tony Ward, University of Montana.

74. Long-term performance of EPA-certified phase 2 woodstove, Klamath Falls

and Portland, Oregon: 1998-1999. 2000. Fisher, Houck, Tiegs (OMNI

Environmental Services) and McGaughey (Eastern Research Group). EPA




76. Nussbaumer T, Klippel N, Johansson L: Survey on measurements and

emission factors on particulate matter from biomass combustion in IEA countries




16th Eurpoean Biomass Conference and Exhibition, 2.- 6.June Valencia, Spain


77. “Inventory of Releases” of dioxins and furans published in 1999 (Environment

Canada, 1999).

78. Residential Wood Combustion – 2000 Source Characterization and Outreach

Efforts. 2009. Anita Wong (Environment Canada). Presentation.

79. Wood Stove Emissions: Particle Size and Chemical Composition. 2000.

McCrillis (US EPA) National Risk Management Research Laboratory, Air

Pollution Prevention and Control Division.

80. Gulland, 2011 (The Wood Heat Organization Inc.)

stories/2011-03-08/acknowledging-human-factor-wood- heating. Accessed April

15, 2014.

81. Emission Factors for New Certified Residential Wood Heaters. 2008. Houck

and Pitzman (OMNI Environmental Services).

82. Peters, A. Air Quality and Cardiovascular Health: Smoke and Pollution

Matter. Circulation. 2009: 120:924-927

83. Baccarelli A., et al. Breathe deeply into your genes!: genetic variants and air

pollution effects. Am J Respir Crit Care Med. 2009 Mar 15;179(6):431-2.

84. Baccarelli A, Wright RO, Bollati V, Tarantini L, Litonjua AA, Suh HH,

Zanobetti A,

Sparrow D, Vokonas PS, Schwartz J. Rapid DNA methylation changes after

exposure to traffic particles. Am J Respir Crit Care Med. 2009 Apr 1;179(7):




87. Geiser M, Rothen-Rutishauser B, Kapp N, Schürch S, Kreyling W, Schulz H,

et al. 2005. Ultrafine Particles Cross Cellular Membranes by Nonphagocytic

Mechanisms in Lungs and in Cultured Cells. Environ Health Perspect

113:1555-1560. doi:10.1289/ehp.8006

88. Bølling A, et al. Health effects of residential wood smoke particles: the

importance of combustion conditions and physicochemical particle propertiesPart

Fibre Toxicol. 2009; 6: 29.

Published online 2009 Nov 6. doi: 10.1186/1743-8977-6-29

89. Tapanainen M, et al. Efficiency of log wood combustion affects the

toxicological and chemical properties of emission particles. Inhal Toxicol. 2012

May;24(6):343-55. doi: 10.3109/08958378.2012.671858.

90. Greenop K, et al. Vehicle refuelling, use of domestic wood heaters and the

risk of childhood brain tumours: Results from an Australian case–control study.

Pediatric Blood & Cancer (Impact Factor: 2.35). 09/2014; DOI: 10.1002/pbc.


91. American Thoracic Society. “Wood smoke exposure multiplies damage from

smoking, increases risk of COPD.” ScienceDaily. ScienceDaily, 16 July 2010.


92. Arrieta O, et al. Clinical and pathological characteristics, outcome and

mutational profiles regarding non-small-cell lung cancer related to wood-smoke

exposure.J Thorac Oncol. 2012 Aug;7(8):1228-34. doi: 10.1097/JTO.


93. Hernández-Garduño E, et al. Wood smoke exposure and lung

adenocarcinoma in non-smoking Mexican women. Int J Tuberc Lung Dis. 2004


94. Javier Pintos J, et al. Use of wood stoves and risk of cancers of the upper

aero-digestive tract: a case-control study. Int. J. Epidemiol. (1998) 27 (6):

936-940 doi:10.1093/ije/27.6.936

95. Perera FP, Tang D, Tu YH, et al. Biomarkers in maternal and newborn blood

indicate heightened fetal susceptibility to procarcinogenic DNA damage. Environ

Health Perspect 2004;112:1133-6.



97. Yap PS, Garcia C. Effectiveness of Residential Wood-Burning Regulation on

Decreasing Particulate Matter Levels and Hospitalizations in the San Joaquin

Valley Air Basin. Am J Public Health. 2015 Feb 25:e1-e7. [Epub ahead of print]




100. Brown AS, et al. Twenty years of measurement of polycyclic aromatic

hydrocarbons in UK ambient air by nationwide air quality networks. Environ Sci

Process Impacts 2013a;15:1199-215.

101. Kim K, et al. A review of airborne polycyclic aromatic hydrocarbons (PAHs)

and their human health effects. Environ Inter. 60 (2013) 71-80.

102. Semmens E, et al. Indoor particulate matter in rural, wood stove heated

homes. Environmental Research 138 (2015) 93–100.

103. Koenig J, and Larson T. A Summary of Emissions Characterization and

Non-Cancer Respiratory Effects of Wood Smoke, USEPA DOC #453/


104. “A Comparison of Source Apportionments of Fine Particulate Matter at Two

San Jose, CA Locations,” from San Jose Speciation Trends Network.

105. Bond, TC, et al. Bounding the role of black carbon in the climate system:

a scientific assessment. Journal of Geophysical Research: Atmospheres.

Volume 118, Issue 11, pages 5380–5552, 16 June 2013



107. Painter T, Deems J, Belnap J, Hamlet A, Landry C, Udall B. Response of

Colorado River runoff to dust radiative forcing in snow. PNAS 2010 107 (40)

17125-17130; published ahead of print September 20, 2010, doi:10.1073/pnas.


108. Yli-Tuomi T, et al. Impact of Wood Combustion for Secondary Heating and

Recreational Purposes on Particulate Air Pollution in a Suburb in Finland.

Environ Sci Technol. 2015 Mar 3. [Epub ahead of print]

109. Burroughs Peña M, Romero KM, Velazquez EJ, Davila-Roman VG, Gilman

RH, Wise RA, Miranda JJ, Checkley W. Relationship Between Daily Exposure to

Biomass Fuel Smoke and Blood Pressure in High-Altitude Peru. Hypertension.

2015 Mar 9. pii: HYPERTENSIONAHA.114.04840. [Epub ahead of print]

110. Peterson B, et al. Effects of Prenatal Exposure to Air Pollutants (Polycyclic

Aromatic Hydrocarbons) on the Development of Brain White Matter, Cognition,

and Behavior in Later Childhood. JAMA Psychiatry. Published online March 25,


111. UNEP/WMO, Integrated Assessment of Black Carbon and

Tropospheric Ozone. Summary for Decision Makers. UN Environment

Program & World Meteorological Organization.

dewa/Portals/67/pdf/Black_Carbon.pdf (accessed 13 March 2012).


112. AAQG. The Most Effective Ways for Individuals to Reduce their

Global Warming. Australian Air Quality Group. Available at: http:// 2014.